DOI: 10.1148/radiol.2402051142
(Radiology 2006;240:574-580.)
© RSNA, 2006
Recent Variceal Bleeding: Doppler US Hepatic Vein Waveform in Assessment of Severity of Portal Hypertension and Vasoactive Drug Response1
Soon Koo Baik, MD, PhD,
Jae Woo Kim, MD,
Hyun Soo Kim, MD, PhD,
Sang Ok Kwon, MD, PhD,
Young Ju Kim, MD,
Joong Wha Park, MD,
Seong Hyun Kim, MD,
Sei Jin Chang, PhD,
Dong Ki Lee, MD, PhD,
Kwang Hyub Han, MD, PhD,
Soon Ho Um, MD, PhD and
Samuel S. Lee, MD, FRCPC
1 From the Departments of Internal Medicine (S.K.B., J.W.K., H.S.K., S.O.K.), Radiology (Y.J.K., J.W.P., S.H.K.), and Preventive Medicine (S.J.C.), Yonsei University Wonju College of Medicine, 162 Ilsan-dong, Wonju 220-701, South Korea; Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea (D.K.L., K.H.H.); Department of Internal Medicine, Korea University College of Medicine, Seoul, South Korea (S.H.U.); and Liver Unit, University of Calgary, Calgary, Alberta, Canada (S.S.L.). Received July 7, 2005; revision requested September 8; revision received September 21; accepted October 18; final version accepted November 23. Supported by the Ministry of Health and Welfare, Republic of Korea (grant A050021) and the Clinical Research Fund of the Korean Association for the Study of the Liver (unencumbered grant from GlaxoSmithKline Korea). S.S.L. supported by an Alberta Heritage Foundation for Medical Research Senior Scholarship award.
Address correspondence to S.K.B. (e-mail: baiksk{at}medimail.co.kr).
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ABSTRACT
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Purpose: To prospectively evaluate both the correlation between abnormal Doppler ultrasonography (US) hepatic vein waveforms and the hepatic venous pressure gradient (HVPG) and the response to drug treatment in patients with cirrhosis.
Materials and Methods: Ethics committee approval and informed consent of patients and control subjects were obtained. In 78 patients with cirrhosis (70 men, eight women; mean age, 49.4 years ± 9.7 [standard deviation]) and a history of variceal bleeding, both the hepatic vein waveform—as measured with Doppler US—and the HVPG were measured, and the relationship between them was analyzed. Hepatic vein Doppler waveforms were classified as triphasic, biphasic, or monophasic. Severe portal hypertension was defined as an HVPG of more than 15 mm Hg. In a subgroup of 21 patients, changes in hepatic vein waveform and HVPG were evaluated after intravenous administration of 2 mg of terlipressin. Statistical analyses were performed with Spearman rank correlation, logistic regression analysis, and cross tabulation.
Results: Abnormal hepatic vein waveforms were seen in 72 patients (92%). Forty-four patients (56%) had biphasic waveforms, 28 (36%) had monophasic waveforms, and six (8%) had triphasic waveforms. A positive correlation was found between the extent of abnormalities in hepatic vein waveforms and the increase in HVPG (P < .05). Monophasic waveforms were associated with severe portal hypertension, with a sensitivity of 74% and a specificity of 95%. Twenty patients in the terlipressin subgroup had abnormal baseline waveforms; the baseline waveform improved in 18 patients in association with the HVPG reduction after injection of terlipressin.
Conclusion: Doppler US hepatic vein waveform assessment is useful in the noninvasive evaluation of the severity of portal hypertension and the response to vasoactive drugs in patients with portal hypertension and variceal bleeding.
© RSNA, 2006
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INTRODUCTION
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Doppler ultrasonography (US) has enabled the noninvasive investigation of hepatic and portal hemodynamics (1–6). Thus, many investigators have attempted to assess portal hypertension with Doppler US in patients with cirrhosis. In particular, any Doppler technique that could be a suitable substitute for the invasive assessment of portal hypertension, such as measurement of the hepatic venous pressure gradient (HVPG), would be highly desirable (7–13). However, at present, both the clinical usefulness and the value of Doppler US in the assessment of portal hypertension remain unsettled (7–9). Doppler indexes that have been commonly used for evaluation of portal hypertension include the measurement of portal and splenic venous blood flow velocity and resistive index of splenic, hepatic, and superior mesenteric arteries. However, these indexes are plagued by a lack of reproducibility and accuracy due to intra- and interobserver variability and interequipment variability (7,14).
The Doppler waveform of the hepatic vein in healthy subjects is normally triphasic (two negative waves and one positive wave) because of central venous pressure variations due to the cardiac cycle (15,16). It has been established that the normal triphasic hepatic vein waveform is transformed into a biphasic or monophasic waveform in patients with cirrhosis (17–23). Moreover, a monophasic waveform has been shown to correlate with a high Child-Pugh score and a poor survival rate (24). Thus, it would be reasonable to hypothesize that abnormalities in the hepatic vein waveform are related to the degree of portal hypertension. To our knowledge, however, no study has been performed to examine a possible correlation between abnormalities in the hepatic vein waveform and the severity of portal hypertension in patients with cirrhosis. Thus, the purpose of our study was to prospectively evaluate both the correlation between abnormal hepatic vein Doppler waveforms and the HVPG and the response to drug treatment in patients with cirrhosis.
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MATERIALS AND METHODS
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Patients and Control Subjects
The ethics committee at Wonju College of Medicine University Hospital approved all components of our study, and patients and control subjects provided written informed consent.
Subjects were drawn from a consecutive series of 126 patients admitted to the Wonju College of Medicine University Hospital with variceal bleeding. Patients were excluded if they did not provide informed consent or if they had hepatocellular carcinoma, severe liver failure (serum bilirubin level >85 µmol/L or hepatic encephalopathy), rebleeding after admission, or thrombosis in the inferior vena cava or a hepatic or portal vein. Seventy-eight patients (70 men, eight women; mean age, 49.4 years ± 9.7 [standard deviation]) were included; none of the patients had congestive heart failure. Cirrhosis was caused by alcohol in 54 patients, by the hepatitis B or C virus in 12, and by a combination of alcohol and the hepatitis B or C virus in seven; cirrhosis was cryptogenic in five patients. Forty-two patients had Child-Pugh class A disease; 28, class B disease; and eight, class C disease.
The 10 control subjects were volunteers from the hospital staff. They had no relevant medical history, and findings of a liver function test, a complete blood count, chest radiography, and electrocardiography were negative for cardiovascular or liver disease. In addition, physical examination findings were normal. The mean age of the five men and five women in the control group was 35.5 years.
Doppler US Examination of the Hepatic Vein
Patients were included in the study 7–10 days after admission and after gastrointestinal bleeding had stopped and hemodynamic conditions had stabilized. No patient took drugs that affected hemodynamics until the initial study was completed. All subjects were studied in the morning after an overnight fast. The hepatic vein Doppler waveform was evaluated within 2 hours before HVPG measurement. To prevent bias, investigators were blinded to the results of the other study. One author (S.K.B., with 7 years of experience with Doppler US of the hepatic vein) performed all hepatic vein waveform studies. Hepatic vein Doppler waveforms were classified and recorded from three repeated measurements. To evaluate interobserver variation, an author (J.W.K., with 3 years experience with hepatic vein waveforms) who was blinded to patient identities reclassified the recorded hepatic vein waveform tracings as triphasic, biphasic, or monophasic for all patients, and the degree of concordance was assessed. We used this nomenclature, which has been used in previous studies, rather than the nomenclature used by Bolondi et al (17).
The reproducibility of this method was evaluated with repeated US studies of hepatic venous flow velocity at the right hepatic vein in the 10 healthy subjects over 5 consecutive days (three repeated measurements were obtained each day) (21). Hepatic vein Doppler US was performed with a previously described method that we modified (17,18,21). After the hepatic vein was depicted along its longitudinal axis with color Doppler flow mapping, Doppler shift signals were obtained in the right hepatic vein at a distance of 3–6 cm from the junction of the hepatic vein and the inferior vena cava. The 3.5-MHz convex probe (SSD-1700; Aloka, Tokyo, Japan) was placed intercostally for optimum recording. Hepatic vein Doppler waveforms were recorded for at least 5 seconds with end-expiration breath holding. In color Doppler flow mapping, a blue hepatic vein waveform indicates flow away from the US probe, whereas a red portal vein waveform indicates flow toward the US probe. We classified the hepatic vein Doppler waveform as triphasic (reversed flow in at least one phase), biphasic (no reversed flow and with or without decreased phasic oscillation), or monophasic (flat and with or without fluttering) (Fig 1) (17,19,20,23). Waveform classification (ie, biphasic or monophasic) depended on the presence or absence of phasic oscillation, which was defined as a regular change in wave amplitude in cadence with the cardiac cycle. A monophasic waveform was defined as complete loss of the normal phasic oscillation (ie, completely flat or with fluttering defined as low-amplitude oscillations, without any variation in amplitude).
HVPG Examination and Evaluation
The HVPG, which was measured during clinical care, was estimated from three repeated measurements, and the mean value was calculated. An examiner (Y.J.K.) with 6 years of experience with HVPG measurement performed all HVPG studies. The coefficient of variation in HVPG measurement is 7% at our center. A catheter was placed percutaneously in the right hepatic vein through the femoral vein, and the pressure in both the wedged position and the free position was recorded with a 7-F balloon-tipped catheter (Arrow Deutschland, Postfach Erding, Germany). The HVPG was determined by subtracting the free hepatic venous pressure from the wedged hepatic venous pressure (1–3). Severe portal hypertension was defined as an HVPG of more than 15 mm Hg (25).
HVPG and Hepatic Vein Waveform before and after Terlipressin Administration
Half of the 78 patients were randomly selected to participate in a substudy of the effects of a single dose of the portal pressure–reducing drug terlipressin. However, only 21 patients agreed to participate in this substudy. The HVPG and hepatic vein waveforms were assessed before (as previously noted) and after intravenous administration of 2 mg of terlipressin (Glypressin; Ferring, Kiel, Germany) (26). Two authors (S.K.B., Y.J.K.) measured hepatic vein waveforms and HVPG, respectively. One author (S.K.B.) interpreted the hepatic vein waveforms obtained before and after terlipressin administration. To evaluate interobserver variation, another author (J.W.K.) performed a second interpretation of hepatic vein waveforms obtained before and after terlipressin administration. The age and sex characteristics of these 21 patients (19 men, two women; mean age, 48.5 years ± 11.1 [standard deviation]) were similar to those of the total group. Cirrhosis was caused by alcohol in 15 patients, by the hepatitis B or C virus in three, and by alcohol and viral hepatitis in two; cirrhosis was cryptogenic in one patient. Both the HVPG and the hepatic vein Doppler waveform were measured before and 20 minutes after intravenous bolus injection of 2 mg of terlipressin. It has been established that the hemodynamic effects of terlipressin are readily demonstrable 20 minutes after intravenous administration (7,27).
Statistical Analysis
The results are expressed as means ± standard deviations. The Spearman rank correlation was used to analyze the relationship between the HVPG and the hepatic vein Doppler waveform. Logistic regression analysis was used to evaluate the relationship between the hepatic vein Doppler waveform and severe portal hypertension. Cross tabulation was used to determine the sensitivity and specificity of the hepatic vein Doppler waveform in patients with severe portal hypertension. We observed the day-to-day variability for 5 consecutive days in 10 healthy control subjects to evaluate intraindividual reproducibility of the hepatic vein Doppler waveform. The coefficient of variation (calculated by dividing the standard deviation by the mean and multiplying by 100) for hepatic vein flow velocity at the right hepatic vein was estimated. A P value of less than .05 was considered to indicate a significant difference. Statistical analysis was performed with software (SPSS for Windows, version 11.0; SPSS, Chicago, Ill).
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RESULTS
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Concordance of Hepatic Vein Doppler Waveform Evaluations
Among the three repeated hepatic vein waveform measurements, concordance in classifying the subtype as triphasic, biphasic, or monophasic was 100%. Concordance between the two observers in classifying the hepatic vein waveforms into three subtypes was 97%. The hepatic vein waveform was triphasic in control subjects. In the control subjects, the coefficient of variation for intraindividual assessment of hepatic vein flow velocity was 10% for the negative flow and 12% for the positive flow; these values are in accordance with published data (21).
Frequency of Abnormalities in Hepatic Vein Doppler Waveform
Of the 78 patients with cirrhosis, 72 (92%) had abnormal changes in the hepatic vein Doppler waveform. Biphasic and monophasic waveforms were seen in 44 (56%) and 28 (36%) patients, respectively; normal triphasic waveforms were noted in six (8%) patients (Table 1).
Relationship between HVPG and Hepatic Vein Doppler Waveform
The mean HVPG was 14.6 mm Hg ± 4.3, and severe portal venous hypertension was observed in 35 (45%) patients. The extent of the hepatic vein Doppler waveform abnormality significantly correlated with the HVPG (Spearman rank correlation coefficient, 0.648; P < .01). An increased frequency of abnormal hepatic vein waveforms was observed with higher HVPGs (Fig 2). Specifically, hepatic vein waveforms showed the disappearance of the normal triphasic waveform and tended to become flat as HVPG increased. Logistic regression analysis showed the monophasic waveform was significantly more likely to be seen in patients with severe portal hypertension than was the triphasic waveform (odds ratio, 28.8; 95% confidence interval: 1.5, 553.8). Moreover, sensitivity and specificity of the monophasic waveform in the diagnosis of severe portal hypertension were 74% and 95%, respectively, as calculated with cross tabulation.
Effect of Terlipressin on HVPG and Hepatic Vein Waveforms
Concordance between the two observers in the interpretation of hepatic vein waveforms before and after administration of terlipressin was 100%. The HVPG decreased in all 21 patients in whom terlipressin was administered; substantial improvements in hepatic vein waveform were detected in 18 patients after terlipressin administration (Table 2) (Fig 3). The baseline hepatic vein waveform was monophasic in 12 patients; however, after terlipressin administration, the hepatic vein waveform in these patients was either biphasic or triphasic. This change was caused by the HVPG decrease. Eight patients had a biphasic hepatic vein waveform at baseline; six of these patients had a triphasic waveform after terlipressin administration. The waveform in the two remaining patients did not conclusively change from biphasic to triphasic; however, an increased amplitude of phasic oscillation, which indicates improvement in the degree of the hepatic vein abnormality, was observed in both subjects after terlipressin administration (Fig 4). One patient showed a constant normal triphasic waveform both before and after terlipressin administration, despite a substantial reduction in HVPG from 19 mm Hg to 5 mm Hg. Overall, 18 (90%) of 20 patients with an abnormal baseline hepatic vein waveform experienced a definitive improvement in waveform type in association with a decrease in HVPG after terlipressin administration (Table 2).
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Figure 3: US images show change in hepatic vein waveform (a) before and (b) 20 minutes after terlipressin administration in a patient with Child-Pugh class B disease. The hepatic vein waveform changed from a monophasic to a biphasic waveform concomitant with a decrease in HVPG from 18 to 9 mm Hg.
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Figure 4: US images show change in hepatic vein waveform (a) before and (b) 20 minutes after terlipressin administration in a patient with Child-Pugh class A disease. Phasic oscillation decreased and biphasic waveform amplitude improved in association with an HVPG decrease from 11 to 7 mm Hg.
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DISCUSSION
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The hepatic vein Doppler waveform in healthy humans is triphasic because of central venous pressure variations that are due to the cardiac cycle (15,16). In patients with cirrhosis, other studies have incontrovertibly demonstrated the presence of abnormal biphasic or monophasic hepatic vein waveforms (17–23). In addition, a previous study showed that the monophasic waveform was correlated with higher Child-Pugh scores and a decreased survival rate (24). However, little is known about the relationship between hepatic vein Doppler waveform abnormalities and portal hypertension. In our study, a correlation was found between abnormalities in the hepatic vein waveform and the HVPG (ie, as HVPG increased, the hepatic vein waveform tended to flatten). Furthermore, the monophasic waveform was associated with severe portal hypertension with relatively high sensitivity and specificity in our study population. Hence, flattening of the hepatic vein waveform in patients with cirrhosis indicates a high likelihood of severe portal hypertension.
Some investigators have suggested classifying the hepatic vein waveform into six subtypes (18,22). In our experience, however, we have found that the availability of this many subtypes leads to greater complexity and larger inter- and intraobserver variability when assigning a subtype to a particular hepatic vein waveform. We believe that the disadvantages associated with the availability of more subtypes outweigh the advantage of a slight improvement in discriminatory ability. Thus, we used a simpler system that we believed was more clinically useful and that had only three subtypes.
Doppler US has been widely used to evaluate abdominal vessels. Although the accuracy and reproducibility of quantitative measurements with Doppler US remains controversial, there is a wider consensus that qualitative US assessment is at least more reproducible, if not more useful, than quantitative indexes (17,28–30). Classification of the hepatic vein Doppler waveform seems to be superior to any quantitative Doppler indexes in terms of reproducibility, technical ease of use, and accuracy. Indeed, the method used for qualitative evaluation of hepatic vein Doppler waveforms is simple enough to potentially allow widespread clinical use. Several previous researchers have examined quantitative methods of assessing the hepatic vein Doppler waveform (15,20,22). However, quantitative measurements of the hepatic vein waveform can be easily influenced by a slight error, which results in poor reproducibility and limits their clinical usefulness (22). Moreover, another drawback of some quantitative hepatic vein waveform measurements is the complexity of the calculation methods. For these reasons, we believe that the present qualitative assessment of the hepatic vein waveform is preferable to any quantitative assessment.
Terlipressin is a synthetic analogue of the vasoconstrictor vasopressin, but it works for a longer period of time and purportedly acts by inducing mesenteric arterial vasoconstriction, thus reducing portal venous flow and portal pressure within minutes (7,25,27). In our study, we evaluated the changes in both hepatic vein waveform and HVPG after terlipressin administration in a subgroup of the study population. Substantial transfiguration in the hepatic vein waveform was found in 18 of 21 patients in association with the HVPG decreases produced with terlipressin administration. In other words, a change in hepatic vein waveform seems to be closely associated with a change in HVPG. Hence, these results indicate that the evaluation of hepatic vein Doppler waveform could be a valuable supplemental tool when assessing the therapeutic response to vasoactive drugs used to treat portal hypertension when HVPG measurement is unfeasible or unavailable. For instance, if a monophasic waveform transformed into a biphasic or triphasic waveform after administration of ß-blockers, one might presume that the ß-blockers reduced the portal pressure.
The exact cause of changes in the hepatic vein Doppler waveform remains unclear. Some investigators have suggested that the hepatic vein wall is thin and surrounded by liver parenchyma so that its compliance can be easily reduced by parenchymal fibrosis and fat infiltration (21,23,24). However, the terlipressin-induced improvement in the waveforms suggests that a hemodynamic effect of high portal pressure rather than a fixed structural abnormality is the pathogenic mechanism responsible for the abnormal waveforms. We believe that high portal pressure probably contributes to the flattening of the normal triphasic hepatic vein waveform by hemodynamically blunting the effect of variations in central venous pressure during the cardiac cycle.
Our study had some limitations. First, one author (S.K.B.) performed Doppler studies of the hepatic vein and classified the results. This could have been a potential weakness when subjective data analysis was performed. However, the 97% concordance of waveform subtypes when assessed by another author reassured us that different observers could reproduce this method of classification. Second, there was a preponderance of men in our study. This was unavoidable, and it reflects the fact that cirrhosis due to alcohol, viral hepatitis, or both, is more prevalent in Korean men. Third, the patients in the terlipressin group were not a true random subset of the overall study group. In this regard, however, their clinical characteristics were not significantly different from those of patients in the larger group. Fourth, we studied only the responses to terlipressin; however, several other drugs are used to treat portal hypertension. Thus, it is not clear if similar patterns of response in hepatic vein waveforms will apply to other therapies, such as administration of ß-blockers. Hence, we suggest that future studies be performed to address these issues.
In conclusion, assessment of the hepatic vein waveform with Doppler US could be considered a useful adjunctive method in the noninvasive assessment of the severity of portal hypertension and the response to vasoactive drugs in patients with portal hypertension and variceal bleeding.
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ADVANCES IN KNOWLEDGE
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- A positive correlation was found between the extent of hepatic vein waveform abnormalities and the hepatic venous pressure gradient increase.
- The monophasic hepatic vein waveform was associated with severe portal hypertension (hepatic venous pressure gradient >15 mm Hg), with 74% sensitivity and 95% specificity.
- After administration of a portal hypotensive drug, improvement in the extent of the hepatic vein waveform abnormality accompanied the decrease in portal pressure.
- Hepatic vein waveform evaluation with Doppler US may be used as a supplemental tool to assess the therapeutic response to portal hypotensive drugs.
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FOOTNOTES
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Abbreviations: HVPG = hepatic venous pressure gradient
Authors stated no financial relationship to disclose.
See also Science to Practice in this issue
Author contributions: Guarantor of integrity of entire study, S.K.B.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; manuscript final version approval, all authors; literature research, J.W.K., S.O.K., S.J.C., S.S.L.; clinical studies, S.K.B., J.W.K., H.S.K., S.O.K., Y.J.K., J.W.P., S.H.K., D.K.L., K.H.H., S.H.U.; statistical analysis, S.K.B., S.J.C.; and manuscript editing, S.K.B., S.O.K., S.J.C., S.S.L.
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ABSTRACT
INTRODUCTION
